OrganismsDiseasesChemicals and DrugsAnalytical, Diagnostic and Therapeutic Techniques and EquipmentPhenomena and ProcessesAnthropology, Education, Sociology and Social PhenomenaHealth Care
ClenbuterolDrug ResiduesAdrenergic beta-AgonistsAdrenergic beta-2 Receptor AgonistsReceptors, Adrenergic, beta-2EthanolaminesFenoterolMethandrostenoloneAnabolic AgentsNandroloneDoping in SportsSteroidsStanozololTachycardia, SupraventricularAtrial FibrillationTachycardia, ParoxysmalDrug OverdoseTachycardiaCatheter AblationEphedrineLipodystrophyLipodystrophy, Congenital GeneralizedHIV-Associated Lipodystrophy SyndromeLipodystrophy, Familial PartialSheepAirway ObstructionLung Diseases, ObstructiveSingle-Blind MethodResidual VolumeBetamethasone ValerateBronchitis
Clenbuterol
A substituted phenylaminoethanol that has beta-2 adrenomimetic properties at very low doses. It is used as a bronchodilator in asthma.
Drug Residues
Drugs and their metabolites which are found in the edible tissues and milk of animals after their medication with specific drugs. This term can also apply to drugs found in adipose tissue of humans after drug treatment.
Adrenergic beta-Agonists
Drugs that selectively bind to and activate beta-adrenergic receptors.
Adrenergic beta-2 Receptor Agonists
Compounds bind to and activate ADRENERGIC BETA-2 RECEPTORS.
Receptors, Adrenergic, beta-2
A subclass of beta-adrenergic receptors (RECEPTORS, ADRENERGIC, BETA). The adrenergic beta-2 receptors are more sensitive to EPINEPHRINE than to NOREPINEPHRINE and have a high affinity for the agonist TERBUTALINE. They are widespread, with clinically important roles in SKELETAL MUSCLE; LIVER; and vascular, bronchial, gastrointestinal, and genitourinary SMOOTH MUSCLE.
Ethanolamines
AMINO ALCOHOLS containing the ETHANOLAMINE; (-NH2CH2CHOH) group and its derivatives.
Fenoterol
An adrenergic beta-2 agonist that is used as a bronchodilator and tocolytic.
Methandrostenolone
A synthetic steroid with anabolic properties that are more pronounced than its androgenic effects. It has little progestational activity. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1188)
Anabolic Agents
These compounds stimulate anabolism and inhibit catabolism. They stimulate the development of muscle mass, strength, and power.
Nandrolone
C18 steroid with androgenic and anabolic properties. It is generally prepared from alkyl ethers of ESTRADIOL to resemble TESTOSTERONE but less one carbon at the 19 position.
Doping in Sports
Illegitimate use of substances for a desired effect in competitive sports. It includes humans and animals.
Steroids
A group of polycyclic compounds closely related biochemically to TERPENES. They include cholesterol, numerous hormones, precursors of certain vitamins, bile acids, alcohols (STEROLS), and certain natural drugs and poisons. Steroids have a common nucleus, a fused, reduced 17-carbon atom ring system, cyclopentanoperhydrophenanthrene. Most steroids also have two methyl groups and an aliphatic side-chain attached to the nucleus. (From Hawley's Condensed Chemical Dictionary, 11th ed)
Stanozolol
A synthetic steroid that has anabolic and androgenic properties. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1194)
Tachycardia, Supraventricular
A generic expression for any tachycardia that originates above the BUNDLE OF HIS.
Atrial Fibrillation
Abnormal cardiac rhythm that is characterized by rapid, uncoordinated firing of electrical impulses in the upper chambers of the heart (HEART ATRIA). In such case, blood cannot be effectively pumped into the lower chambers of the heart (HEART VENTRICLES). It is caused by abnormal impulse generation.
Tachycardia, Paroxysmal
Abnormally rapid heartbeats with sudden onset and cessation.
Drug Overdose
Accidental or deliberate use of a medication or street drug in excess of normal dosage.
Tachycardia
Abnormally rapid heartbeat, usually with a HEART RATE above 100 beats per minute for adults. Tachycardia accompanied by disturbance in the cardiac depolarization (cardiac arrhythmia) is called tachyarrhythmia.
Catheter Ablation
Removal of tissue with electrical current delivered via electrodes positioned at the distal end of a catheter. Energy sources are commonly direct current (DC-shock) or alternating current at radiofrequencies (usually 750 kHz). The technique is used most often to ablate the AV junction and/or accessory pathways in order to interrupt AV conduction and produce AV block in the treatment of various tachyarrhythmias.
Ephedrine
A phenethylamine found in EPHEDRA SINICA. PSEUDOEPHEDRINE is an isomer. It is an alpha- and beta-adrenergic agonist that may also enhance release of norepinephrine. It has been used for asthma, heart failure, rhinitis, and urinary incontinence, and for its central nervous system stimulatory effects in the treatment of narcolepsy and depression. It has become less extensively used with the advent of more selective agonists.
Lipodystrophy
A collection of heterogenous conditions resulting from defective LIPID METABOLISM and characterized by ADIPOSE TISSUE atrophy. Often there is redistribution of body fat resulting in peripheral fat wasting and central adiposity. They include generalized, localized, congenital, and acquired lipodystrophy.
Lipodystrophy, Congenital Generalized
Congenital disorders, usually autosomal recessive, characterized by severe generalized lack of ADIPOSE TISSUE, extreme INSULIN RESISTANCE, and HYPERTRIGLYCERIDEMIA.
HIV-Associated Lipodystrophy Syndrome
Defective metabolism leading to fat maldistribution in patients infected with HIV. The etiology appears to be multifactorial and probably involves some combination of infection-induced alterations in metabolism, direct effects of antiretroviral therapy, and patient-related factors.
Lipodystrophy, Familial Partial
Inherited conditions characterized by the partial loss of ADIPOSE TISSUE, either confined to the extremities with normal or increased fat deposits on the face, neck and trunk (type 1), or confined to the loss of SUBCUTANEOUS FAT from the limbs and trunk (type 2). Type 3 is associated with mutation in the gene encoding PEROXISOME PROLIFERATOR-ACTIVATED RECEPTOR GAMMA.
Sheep
Any of the ruminant mammals with curved horns in the genus Ovis, family Bovidae. They possess lachrymal grooves and interdigital glands, which are absent in GOATS.
Airway Obstruction
Any hindrance to the passage of air into and out of the lungs.
Lung Diseases, Obstructive
Any disorder marked by obstruction of conducting airways of the lung. AIRWAY OBSTRUCTION may be acute, chronic, intermittent, or persistent.
Single-Blind Method
A method in which either the observer(s) or the subject(s) is kept ignorant of the group to which the subjects are assigned.
Residual Volume
The volume of air remaining in the LUNGS at the end of a maximal expiration. Common abbreviation is RV.
Betamethasone Valerate
The 17-valerate derivative of BETAMETHASONE. It has substantial topical anti-inflammatory activity and relatively low systemic anti-inflammatory activity.
Bronchitis
Inflammation of the large airways in the lung including any part of the BRONCHI, from the PRIMARY BRONCHI to the TERTIARY BRONCHI.

beta2-adrenergic receptor-selective agonist clenbuterol prevents Fas-induced liver apoptosis and death in mice. (1/192)

Stimulation of the cAMP-signaling pathway modulates apoptosis in several cell types and inhibits Jo2-mediated apoptosis in cultured rat hepatocytes. No information is yet available as to whether the hepatic beta2-adrenergic receptor (AR) expression level, including beta2-AR-dependent adenylyl cyclase activation, modulates hepatocyte sensitivity to apoptosis in vivo or whether this sensitivity can be modified by beta2-AR ligands. We have examined this using C57BL/6 mice, in which hepatic beta2-AR densities are low, and transgenic F28 mice, which overexpress beta2-ARs and have elevated basal liver adenylyl cyclase activity. The F28 mice were resistant to Jo2-induced liver apoptosis and death. The beta-AR antagonist propranolol sensitized the F28 livers to Jo2. In normal mice clenbuterol, a beta2-AR-specific agonist, considerably reduced Jo2-induced liver apoptosis and death; salbutamol, another beta2-AR-selective agonist, also reduced Jo2-induced apoptosis and retarded death but with less efficacy than clenbuterol; and propranolol blocked the protective effect of clenbuterol. This indicates that the expression level of functional beta2-ARs modulates Fas-regulated liver apoptosis and that this apoptosis can be inhibited in vivo by giving beta2-AR agonists. This may well form the basis for a new therapeutic approach to diseases involving abnormal apoptosis.  (+info)

Study of interaction between agonists and asn293 in helix VI of human beta(2)-adrenergic receptor. (2/192)

Previously, we demonstrated the involvement of Asn293 in helix VI of the human beta(2)-adrenergic receptor in stereoselective agonist recognition and activation. In the present study, we have further explored the role of this residue by synthesizing derivatives of isoproterenol and clenbuterol, two beta-adrenergic receptor agonists. We analyzed their efficacy and affinity on the wild-type and a mutant receptor (Asn293Leu). Each compound had similar efficacy (tau values) on both the wild-type and mutant receptor, although tau values varied considerably among the eight compounds studied. It appeared that one derivative of isoproterenol, but not of clenbuterol, showed a gain in affinity from the wild type to the mutant receptor. This derivative had a methyl substituent instead of the usual beta-OH group in the aliphatic side chain of isoproterenol, compatible with the more lipophilic nature of the leucine side chain. Such a "gain of function" approach through a combination of synthetic chemistry with molecular biology, may be useful to enhance our insight into the precise atomic events that govern ligand-receptor interactions.  (+info)

Rapid extraction of clenbuterol from human and calf urine using empore C8 extraction disks. (3/192)

In the present paper, disk extraction was evaluated for the rapid isolation of clenbuterol from human and calf urine, followed by high-performance liquid chromatography analysis with UV detection. A method was developed for the extraction with standard density C8 disks. The disks could be washed with 25% methanol in 0.01M sodium hydroxide without significant losses of clenbuterol. The recovery of denbuterol was about 85%, and the extracts were clean. The detection limit was about 10 ng/mL. The main advantages of these disks were the saving of time and the reduced amounts of organic solvents needed.  (+info)

Deleterious effects of chronic clenbuterol treatment on endurance and sprint exercise performance in rats. (4/192)

The beta(2)-adrenergic agonist, clenbuterol, has powerful muscle anabolic and lipolytic effects and is used by athletes to improve exercise performance; however, its use in conjunction with different forms of exercise training has received limited attention. Since previous studies have reported that chronic use of other beta(2)-adrenergic agonists has deleterious effects on cardiac muscle structure and function, the aim of the present study was to determine whether chronic clenbuterol administration would reduce the exercise capabilities of rats subjected to long-term treadmill sprint running, endurance swimming or voluntary wheel running training. The effect of clenbuterol treatment on exercise performance in rats was evaluated in three separate studies. Different groups of male rats were assigned to an endurance swimming (2 h/day, 5/7 days, 18 weeks) group, a treadmill sprint running (8x1 min bouts, 1.05 m/s, 20 weeks) group, or a voluntary wheel running (16 weeks) group. In each study, rats were allocated into either a treated group that received clenbuterol (2 mg.kg(-1).day(-1)) in their drinking water or an untreated control group. In each of the three studies, treated rats exhibited a reduction in exercise performance compared with untreated rats. Treated rats ran approximately 57% less total distance than untreated rats in the voluntary running programme and were unable to complete the swimming and sprinting protocols performed by the untreated rats. In each of the studies, the treated rats exhibited cardiac hypertrophy, with absolute heart mass increased by approximately 19% and heart mass relative to body mass increased by approximately 20%. The hearts of sedentary rats treated with clenbuterol exhibited extensive collagen infiltration surrounding blood vessels and in the wall of the left ventricle. The results indicate strongly that chronic clenbuterol administration deleteriously affects exercise performance in rats, potentially due to alterations in cardiac muscle structure and function.  (+info)

Effects of beta(2)-agonist clenbuterol on biochemical and contractile properties of unloaded soleus fibers of rat. (5/192)

The effects of clenbuterol beta(2)-agonist administration were investigated in normal and atrophied [15-day hindlimb-unloaded (HU)] rat soleus muscles. We showed that clenbuterol had a specific effect on muscle tissue, since it reduces soleus atrophy induced by HU. The study of Ca(2+) activation properties of single skinned fibers revealed that clenbuterol partly prevented the decrease in maximal tension after HU, with a preferential effect on fast-twitch fibers. Clenbuterol improved the Ca(2+) sensitivity in slow- and fast-twitch fibers by shifting the tension-pCa relationship toward lower Ca(2+) concentrations, but this effect was more marked after HU than in normal conditions. Whole muscle electrophoresis indicated slow-to-fast transitions of the myosin heavy chain isoforms for unloaded and for clenbuterol-treated soleus. The coupling of the two latter conditions did not, however, increase these phenotypical transformations. Our findings indicated that clenbuterol had an anabolic action and a beta(2)-adrenergic effect on muscle fibers and appeared to counteract some effects of unloading disuse conditions.  (+info)

Differential effects of dexamethasone and clenbuterol on rat growth and on beta2-adrenoceptors in lung and skeletal muscle. (6/192)

Beta-adrenergic agonists increase growth rate, but their efficacy is reduced over time as the number of beta2-adrenoceptors in muscle decreases. Dexamethasone increases beta2-adrenoceptor density in many tissues, but this effect has not been reported in skeletal muscle. In this study, male rats were treated daily for 10 d with either clenbuterol (4 mg/kg of feed), dexamethasone (.2 mg/kg BW, s.c.), or clenbuterol plus dexamethasone. Untreated rats served as controls. Dexamethasone caused a marked suppression of growth rate, which resulted in decreased (P < .001) body weight (-29%), carcass weight (-30%), hind-limb muscles (-22%), omental fat (-22%), and heart weight (-10%). Feed intake was reduced (-26%), but feed conversion efficiency was also impaired (P < .001). Clenbuterol caused a small increase in growth rate (+6%; P < .05), with an increase in leg muscle (+7%; P < .01) and heart mass (+8%; P < .05). Feed efficiency was improved (P < .001) by clenbuterol. Rats given the combined treatment still showed a reduction in growth rate (-81%). Clenbuterol caused only a mild attenuation of the effects of dexamethasone on feed intake, BW, and carcass weight, but reduced the catabolic effect of dexamethasone on hind-limb muscle to only -8%. Clenbuterol caused a slight increase in the affinity beta2-adrenoceptors in lung for binding to the radioligand (-)[125I]iodocyanopindolol. Relative to control values, the density of beta2-adrenoceptors in lung was +31% with dexamethasone treatment, -45% with clenbuterol, and -23% with the combined treatment. Clenbuterol also decreased beta2-adrenoceptors in skeletal muscle (-35%), but so did dexamethasone (-13%), so the effects of the beta-adrenergic agonist were not attenuated through use of the combined treatment (-40%). The results show that the inductive effect of glucocorticoids on beta2-adrenoceptors is tissue-specific and that glucocorticoid treatment is not a useful adjunct to beta-adrenergic agonist treatment in animal production.  (+info)

Power output of fast and slow skeletal muscles of mdx (dystrophic) and control mice after clenbuterol treatment. (7/192)

The mdx mouse is the most commonly used animal model for Duchenne muscular dystrophy. We tested the null hypothesis that 20 weeks of clenbuterol treatment ( approximately 2 mg kg-1 day-1) of mdx and control mice would have no effect on the absolute and specific force (Po, kN m-2) and absolute and normalised power output (W kg-1) of extensor digitorum longus (EDL) and soleus muscles. For mdx and control mice, clenbuterol treatment produced modest increases in the mass of the two muscles but did not increase absolute or specific force or normalised power output. For absolute power output, only the EDL muscles of mdx mice showed a difference following treatment, with the power output of treated mice being 118 % that of the untreated mice. The modest effects of clenbuterol treatment on the dynamic properties of skeletal muscle provide little support for any improvement in muscle function for the dystrophic condition.  (+info)

Function and distribution of beta3-adrenoceptors in rat, rabbit and human urinary bladder and external urethral sphincter. (8/192)

1. Activation of beta-adrenoceptors causes relaxation of the urinary bladder and contraction of the external urethral sphincter, which consists of fast-contracting skeletal muscles. A beta2-adrenoceptor agonist, clenbuterol, recently has been developed as a therapeutic drug for the treatment of urinary incontinence, however beta2-adrenoceptor agonists have undesirable effects on cardiac and striated muscle function. 2. In this study, we compared the effects of the beta2-adrenoceptor agonist, clenbuterol and of a novel beta3-adrenoceptor agonist, GS332, on urinary bladder and external urethral sphincter function in rat, rabbit and human. We also determined the distribution of beta3-adrenoceptors in human urinary bladder and external urethral sphincter, using radioligand-binding techniques. 3. Clenbuterol induced marked relaxations in rat, rabbit and human urinary bladder smooth muscles and also induced marked contractions in rat periurethral striated muscles (external urethral sphincter), while GS332 induced marked relaxations in rat and human, but not in rabbit, urinary bladder smooth muscles and induced small contractions in rat periurethral striated muscles. 4. The radioligand binding studies showed presence of beta2- and beta3-adrenoceptors in human urinary bladder, external urethral sphincter and abdominal rectus muscles. The affinities of GS332 were the highest in urinary bladder and the lowest in the skeletal (abdominal rectus) muscles, while the affinities of clenbuterol were similar in urinary bladder, external urethral sphincter and the skeletal (abdominal rectus) muscles. 5. These results suggest that GS332 could, similarly clenbuterol, have a role in the treatment of urinary frequency and urinary incontinence.  (+info)

β2-Agonist clenbuterol suppresses bacterial phagocytosis of splenic macrophages expressing high levels of macrophage receptor...β2-Agonist clenbuterol suppresses bacterial phagocytosis of splenic macrophages expressing high levels of macrophage receptor...
TY - JOUR. T1 - β2-Agonist clenbuterol suppresses bacterial phagocytosis of splenic macrophages expressing high levels of macrophage receptor with collagenous structure. AU - Shirato, Ken. AU - Sato, Shogo. AU - Sato, Madoka. AU - Hashizume, Yoko. AU - Tachiyashiki, Kaoru. AU - Imaizumi, Kazuhiko. PY - 2013/3. Y1 - 2013/3. N2 - Splenic marginal zone macrophages expressing macrophage receptor with collagenous structure (MARCO) contribute to the clearance of blood-borne pathogens. We determined a splenic adherent cell fraction abundantly containing cells expressing a higher level of MARCO by flow cytometry, and examined the effects of daily administration of an anabolic dose of β2-agonist clenbuterol on the phagocytic capacity of the cells in mice. After 6 weeks of clenbuterol (1.0 mg/kg body weight/d) or vehicle administration to the mice, splenic adherent cells were isolated. These cells were separated into three cell-size subpopulations. Among them, the small-cell subpopulation contained ...
https://waseda.pure.elsevier.com/en/publications/%CE%B22-agonist-clenbuterol-suppresses-bacterial-phagocytosis-of-splen
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Beneficial wound healing and metabolic effects of clenbuterol in burned and nonburned rats<...Beneficial wound healing and metabolic effects of clenbuterol in burned and nonburned rats<...
TY - JOUR. T1 - Beneficial wound healing and metabolic effects of clenbuterol in burned and nonburned rats. AU - Hollyoak, Maureen A.. AU - Muller, Michael J.. AU - Meyers, Nicholas A.. AU - Williams, William G.. AU - Barrow, Robert E.. AU - Herndon, David N.. PY - 1995/1/1. Y1 - 1995/1/1. N2 - Clenbuterol is known to increase muscle mass in nonburned and burn-injured subjects. The effects of clenbuterol on wound healing and the postburn response were examined in both nutritionally matched and free-feeding groups of rats. Rats received either a sham or 30% total body surface area scald burn and then a dorsal incision. Clenbuterol (2 mg/kg/day) was administered subcutaneously via a miniosmotic pump. The burn injury resulted in a sustained non-temperature-dependent hypermetabolism that was not altered by clenbuterol. Clenbuterol induced muscle anabolism and body growth in sham and burned-injured animals. Treated sham animals demonstrated increased wound breaking strength. Matched nutritional ...
https://researchexperts.utmb.edu/en/publications/beneficial-wound-healing-and-metabolic-effects-of-clenbuterol-in-
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Muscle protein waste in tumor-bearing rats is effectively antagonized by a beta 2-adrenergic agonist (clenbuterol). Role of the...Muscle protein waste in tumor-bearing rats is effectively antagonized by a beta 2-adrenergic agonist (clenbuterol). Role of the...
Tissue protein hypercatabolism (TPH) is a most important feature in cancer cachexia, particularly with regard to the skeletal muscle. The rat ascites hepatoma Yoshida AH-130 is a very suitable model system for studying the mechanisms involved in the processes that lead to tissue depletion, since it induces in the host a rapid and progressive muscle waste mainly due to TPH (Tessitore, L., G. Bonelli, and F. M. Baccino. 1987. Biochem. J. 241:153-159). Detectable plasma levels of tumor necrosis factor-alpha associated with marked perturbations in the hormonal homeostasis have been shown to concur in forcing metabolism into a catabolic setting (Tessitore, L., P. Costelli, and F. M. Baccino. 1993. Br. J. Cancer. 67:15-23). The present study was directed to investigate if beta 2-adrenergic agonists, which are known to favor skeletal muscle hypertrophy, could effectively antagonize the enhanced muscle protein breakdown in this cancer cachexia model. One such agent, i.e., clenbuterol, indeed largely ...
http://www.recercat.cat/handle/2072/227235
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Negative effect of clenbuterol on physical capacities and neuromuscular control of muscle atrophy in adult rats. - Etap LabNegative effect of clenbuterol on physical capacities and neuromuscular control of muscle atrophy in adult rats. - Etap Lab
INTRODUCTION: Clenbuterol has been used to alleviate chronic obstructive pulmonary disease and elicit an anabolic response in muscles. The aim of this study was to determine the influence of muscle mass variation on physical capacities in rats.. METHODS: The left hindlimbs of Wistar rats were immobilized for 20 days in plantarflexion with a splint and then remobilized for 16 days. The effect of a non-myotoxic dose of clenbuterol during the immobilization period was evaluated. Physical capacities were coordination, free locomotion, grip strength, and bilateral deficit.. RESULTS: Immobilization induced a loss of muscle mass, coordination, and strength without any effect on free locomotion. The positive anabolic effect of clenbuterol did not prevent a loss of physical capacities resulting from immobilization.. CONCLUSIONS: Muscle mass correlated strongly with coordination and isometric strength in untreated rats. Anabolic effect, fiber phenotype modification, and perturbation in neuromuscular ...
http://www.etap-lab.com/publications/negative-effect-of-clenbuterol-on-physical-capacities-and-neuromuscular-control-of-muscle-atrophy-in-adult-rats/
Amelioration of denervation-induced atrophy by clenbuterol is associated with increased PKC-alpha activity<...Amelioration of denervation-induced atrophy by clenbuterol is associated with increased PKC-alpha activity<...
TY - JOUR. T1 - Amelioration of denervation-induced atrophy by clenbuterol is associated with increased PKC-alpha activity. AU - Sneddon, Alan Arthur. AU - Delday, Margaret Inkster. AU - Maltin, Charlotte. PY - 2000/7. Y1 - 2000/7. N2 - Rat soleus muscle was denervated for 3 or 7 days, and total membrane protein kinase C (PKC) activity and translocation and immunocytochemical localization of PKC isoforms were examined. Dietary administration of clenbuterol concomitant with denervation ameliorated the atrophic response and was associated with increased membrane PKC activity at both 3 (140%) and 7 (190%) days. Of the five PKC isoforms (alpha, epsilon, theta, zeta, and mu) detected in soleus muscle by Western immunoblotting, clenbuterol treatment affected only the PKC-alpha and PKC-theta forms. PKC-alpha was translocated to the membrane fraction upon denervation, and the presence of clenbuterol increased membrane-bound PKC-alpha and active PKC-alpha as assayed by Ser(657) phosphorylation. PKC-theta ...
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  • The action of clenbuterol is primarily highly anti-catabolic, and the proportion in which the proteins are removed from the muscle cells, is reduced, which causes an increase in the size of these cells. (2getmass.to)
  • Clenbuterol is known to increase muscle mass in nonburned and burn-injured subjects. (utmb.edu)
  • Clenbuterol elevated RNA concentration in the tibialis muscle and reduced it in the liver. (utmb.edu)
Drug5
  • WILLIAMS DA Examining potential drug therapies for muscular dystrophy utilising the dy/dy mouse: I. Clenbuterol. (pro.br)
  • Clenbuterol is banned for use by IOC tested athletes and it is not approved for human consumption by the Food and Drug Administration in the United States. (geekbarchicago.com)
  • Nowadays, the use of a clenbuterol cycle has become even more popular, thanks to the many A-list celebrities who have been reported to be using the said drug. (wordpress.com)
  • But beyond its benefits on breathing, Clenbuterol has managed to become the most popular drug for effective fat loss. (2getmass.to)
  • These results suggest that the utilization of clenbuterol as doping drug impairs bacterial clearance in the spleen. (elsevier.com)
Weight3
  • Anyone considering use of legal Clenbuterol for weight loss should be aware that it will not work without a nutritious and balanced diet and appropriate exercise. (steroidio.com)
  • Even so, other specific prescription weight-loss drugs may work more efficiently in this regard than Clenbuterol. (steroidio.com)
  • In addition to Clenbuterol steroids, it is also possible to buy Clenbuterol weight loss products. (ilmuseums.com)
Athletes2
  • Why would bodybuilders and athletes use Clenbuterol? (steroidio.com)
  • Because of the mechanism of action of widening or dilating the smooth muscular tissues of the bronchi inside the lungs, athletes perceive that Clenbuterol will also increase oxygen intake. (steroidio.com)
Ketotifen1
  • citation needed] However, ketotifen z clenbuterol this is a biased estimator, as the estimates are generally too low? (badgesports.com)
Results2
  • Clenbuterol, reviews and Results How to take. (baafi281.pro)
  • Results: Administration of clenbuterol (p.o.) one hour before, or intravenous at the same time as LPS-challenge resulted in a marked reduction of plasma levels of TNFα, IL-1β, and IL-6. (tudelft.nl)
Catabolic2
  • Another benefit that spurs people to purchase clenbuterol online is both its anabolic and catabolic properties that it possesses. (wordpress.com)
  • Clenbuterol may prove beneficial in patients with severe prolonged catabolic state, such as that associated with burn injury, by promoting protein anabolism and enhancing wound healing. (utmb.edu)
Tissue1
  • Clenbuterol minimized LPS-induced liver damage, as represented by significantly lowered concentrations of several parameters for liver-failure (AST, ALT, Bilirubin), and improved hepatic tissue morphology. (tudelft.nl)